ライフサイエンスコーパス: bacterial sepsis

1 ected neutropenic rats against gram-negative bacterial sepsis.

2 may prove a promising treatment strategy for bacterial sepsis.

3 tritional supplementation was detrimental in bacterial sepsis.

4 cause of the high mortality associated with bacterial sepsis.

5 ti-organ failure contributes to mortality in bacterial sepsis.

6 ere unable to mount trained immunity against bacterial sepsis.

7 l killing, we determined the role of DJ-1 in bacterial sepsis.

8 inflammation and greater than 2.0 ng/ml for bacterial sepsis.

9 moniae are a frequent cause of Gram-negative bacterial sepsis.

10 critical role in the pathogenesis of severe bacterial sepsis.

11 is a key event in neonatal susceptibility to bacterial sepsis.

12 produce IL-10 is a risk factor for neonatal bacterial sepsis.

13 ection and died from fulminant gram-positive bacterial sepsis.

14 ng cause of human soft tissue infections and bacterial sepsis.

15 tective early innate immune responses during bacterial sepsis.

16 s in the early innate immune response during bacterial sepsis.

17 he cytokine storm caused by TLR agonists and bacterial sepsis.

18 identify patients at high risk of developing bacterial sepsis.

19 vival benefit in both experimental models of bacterial sepsis.

20 , compromised wound integrity, and increased bacterial sepsis.

21 id bacterial identification in patients with bacterial sepsis.

22 endotoxin but has not been evaluated during bacterial sepsis.

23 ial cell death associated with Gram-negative bacterial sepsis.

24 everity of necrotizing enterocolitis, and/or bacterial sepsis.

25 d that this reactivation can be triggered by bacterial sepsis.

26 system, similar to those reported in severe bacterial sepsis.

27 a bacterial pathogen and predisposes mice to bacterial sepsis.

28 onents that function coordinately to prevent bacterial sepsis.

29 t, if not all, of the events associated with bacterial sepsis.

30 ol patients and patients dying from systemic bacterial sepsis.

31 by macrophages which occurs in Gram-negative bacterial sepsis.

32 lung, and resembles the clinical picture of bacterial sepsis.

33 involvement in the inflammatory response to bacterial sepsis.

34 TNFalpha results in many of the hallmarks of bacterial sepsis.

35 of the association between this variant and bacterial sepsis.

36 mortality was higher (68%) for patients with bacterial sepsis.

37 ts obtained for neonates suspected of having bacterial sepsis.

38 reveals a potential avenue for treatment in bacterial sepsis.

39 patients or experimental animals undergoing bacterial sepsis.

40 By contrast, in a mouse model of bacterial sepsis after intraperitoneal inoculation of GA

41 Transfusion-related bacterial sepsis, although infrequent, is a serious and

42 d hypotension (both resolved), and 1 died of bacterial sepsis and acute respiratory distress syndrome

43 uent and associated with the cooccurrence of bacterial sepsis and clinically significant pneumothorax

44 ociated with an increased risk of nosocomial bacterial sepsis and coagulase negative staphylococcal i

45 developed progressive pulmonary failure and bacterial sepsis and died.

46 nclude that dantrolene decreases survival in bacterial sepsis and has no effect on survival in endoto

47 Despite extensive research, bacterial sepsis and its associated systemic inflammatio

48 Streptococcus (GBS) is the leading cause of bacterial sepsis and meningitis among neonates.

49 ptococcus agalactiae is the leading cause of bacterial sepsis and meningitis among newborns.

50 B Streptococcus (GBS) is a leading cause of bacterial sepsis and meningitis in newborns.

51 scherichia coli is a major cause of neonatal bacterial sepsis and meningitis.

52 g, including increased incidence of neonatal bacterial sepsis and necrotizing enterocolitis.

53 There was a smaller impact on bacterial sepsis and pneumonia, and an increase observed

54 in coordinating complex immune responses to bacterial sepsis and suggests that future strategies for

55 theless, the exact status of NK cells during bacterial sepsis and their capacity directly to respond

56 systemic inflammatory response syndromes in bacterial sepsis and viral haemorrhagic fevers, and anti

57 he inhibition of TNF-alpha production during bacterial sepsis are critical in attenuating adverse hos

58 Immunosuppression and bacterial sepsis are thought to stimulate reactivation o

59 Studies that define natural responses to bacterial sepsis assumed new relevance after the lethal

60 Males are more prone to bacterial sepsis, but some studies suggest females may h

61 Our recent work has shown that polymicrobial bacterial sepsis can trigger reactivation of latent muri

62 Bacterial sepsis caused significant maldistribution of i

63 Gram-negative bacterial sepsis commonly causes organ dysfunction and d

64 efore therapy, another died with concomitant bacterial sepsis during induction therapy.

65 tween cytokine gene polymorphisms and severe bacterial sepsis, have reached conflicting conclusions.

66 nduction course complicated by Gram-negative bacterial sepsis, her counts recovered by day 32, and bo

67 Using a well-established model of bacterial sepsis in Drosophila melanogaster, we found th

68 dotoxin in the pathogenesis of Gram-negative bacterial sepsis in preclinical investigations and numer

69 GBS) infections are the most common cause of bacterial sepsis in the immediate newborn period.

70 The current standard of care for evaluating bacterial sepsis in the newborn is performing blood cult

71 the role of the endothelial selectins during bacterial sepsis in vivo, Streptococcus pneumoniae (1-10

72 Bacterial sepsis involves a complex interaction between

73 Bacterial sepsis is a major cause of neonatal morbidity

74 Transfusion-associated bacterial sepsis is a persistent problem in transfusion

75 Bacterial sepsis is a serious life-threatening condition

76 Thus, the benefit of B-1a cells in bacterial sepsis is mediated by CREB and the identificat

77 An important site of cellular damage in bacterial sepsis is mitochondrial DNA (mtDNA), which we

78 to transfusion-related acute lung injury and bacterial sepsis is not suspected, the correct diagnosis

79 The morbidity associated with bacterial sepsis is the result of host immune responses

80 Under conditions of bacterial sepsis, large amounts of NO are produced, caus

81 Severe bacterial sepsis leads to a proinflammatory condition th

82 y immune responses and oxidant stress during bacterial sepsis {lsqb;i.e., cecal ligation and puncture

83 hypothesize that MCMV reactivation following bacterial sepsis may be caused by inflammatory mediators

84 Procalcitonin (PCT), a marker of bacterial sepsis, may also act as a mediator of the infl

85 Thus, during Gram-negative bacterial sepsis Mkp-1 not only plays a critical role in

86 ts died in complete remission as a result of bacterial sepsis (n = 2), chronic GVHD and fungal infect

87 idered possibly related to momelotinib], and bacterial sepsis [n=1]); and four patients (8%) receivin

88 Transient neutropenia/thrombocytopenia, bacterial sepsis, neurotoxicity, stomatitis, and hospita

89 rate that the detrimental immune response to bacterial sepsis occurs via TLR9 stimulation.

90 Severe bacterial sepsis often leads to a systemic procoagulant

91 reptococcus agalactiae, the leading cause of bacterial sepsis, pneumonia, and meningitis in neonates

92 apy or as a single agent in animal models of bacterial sepsis, rats were implanted intraperitoneally

93 virus infection but - similar to findings in bacterial sepsis - reduction of inflammation, rather tha

94 The roles of miRNAs in host defense against bacterial sepsis remain unclear.

95 Identifying patients at high risk for bacterial sepsis remains an important clinical challenge

96 tensive research into the mechanisms driving bacterial sepsis, the target molecules controlling vascu

97 enectomy are considered at increased risk of bacterial sepsis, they typically receive vaccination, ed

98 f commonly encountered diseases ranging from bacterial sepsis to sterile syndromes such as major trau

99 Bacterial sepsis triggers robust activation of the compl

100 tion in 10 premature infants with documented bacterial sepsis was then followed for 2 to 12 weeks aft

101 Using a mouse model of bacterial sepsis, we found that the numbers of B-1a cell